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通过蠕变性能的测试和内摩擦应力的测定,研究了[001]、[011]和[111]取向镍基单晶高温合金分别沿[001]、[011]和[111]取向在高温/低应力条件下拉伸蠕变至稳态阶段的有效蠕变参数及其与蠕变性能和变形机制之间的关系。结果表明,随着温度的升高和外加应力的降低,3种取向合金的内摩擦应力降低。在相同条件下,3种取向合金的内摩擦应力顺序为σ_(i[001])>σ_(i[111])>σ_(i[011])。蠕变前后[011]和[111]取向合金内相对于应力轴倾斜连贯的“屋脊”型基体通道是2种合金具有较低内摩擦应力和较差蠕变抗力的重要原因。[001]取向合金在1040℃/137 MPa条件下的有效蠕变激活能为Q_(e[001])=281.32 kJ/mol,表明其稳态阶段的变形机制为元素扩散控制的位错攀移。[011]取向合金的有效蠕变激活能为Q_(e[011])=146.87 kJ/mol,其较低的数值与其内部开放的基体通道对位错滑移较小的阻碍作用有关;[111]取向合金较[011]取向合金较高的有效蠕变激活能Q_(e[111])=182.61 kJ/mol与其内部片层状的γ′相和位错的交滑移有关。
Through the testing of creep property and the determination of internal friction stress, the effects of [001], [011] and [111] oriented nickel base single crystal superalloys on [001], [011] and [111] The Effective Creep Parameters from Tensile Creep to Steady State in Low Stress Conditions and Their Relationship with Creep Properties and Deformation Mechanisms. The results show that with the increase of temperature and the decrease of the applied stress, the internal friction stresses of the three kinds of oriented alloys decrease. Under the same conditions, the internal frictional stress order of the three kinds of oriented alloys is σ_ (i [001])> σ_ (i [111])> σ_ (i [011]). The “ridge ” type matrix channel in the [011] and [111] oriented alloys, which are inclined and coherent with respect to the stress axis before and after creep, is the main reason for the two alloys having lower internal friction and lower creep resistance. The effective creep activation energy of [001] oriented alloy at 1040 ℃ / 137 MPa is Q_ (e [001]) = 281.32 kJ / mol, indicating that the deformation mechanism of the [001] orientation alloy is elemental diffusion controlled dislocation climbing . The effective creep activation energy of the oriented alloy is Q e (011) = 146.87 kJ / mol, and its lower value is related to the less hindered dislocation slip of the open-oriented matrix channels. The higher effective creep activation energy Q_ (e [111]) = 182.61 kJ / mol than that of the [011] oriented alloy is related to the cross-slip of its internal lamellar γ ’phase and dislocations.